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Melatonin attenuates gentamicin-induced nephrotoxicity and oxidative stress in rats
In-Chul Lee1, Sung-Hwan Kim, Sang-Min Lee
1College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Republic of Korea.
Abstract:
The present study investigated the protective effects of melatonin (MT) against gentamicin (GM)-induced nephrotoxicity and oxidative stress in rats. We also investigated the effects of MT on induction of apoptotic cell death and its potential mechanisms in renal tissues in response to GM treatment. The following four experimental groups were evaluated: (1) vehicle control, (2) MT (15 mg/kg/day), (3) GM (100 mg/kg/day), and (4) GM&MT. GM caused severe nephrotoxicity as evidenced by increased serum blood urea nitrogen and creatinine levels, increased renal tubular cell apoptosis, and increased Bcl2-associated X protein and cleaved caspase-3 protein expression. Additionally, GM treatment caused an increase in levels of inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-κB) protein expression in renal tissues. The significant decreases in glutathione content, catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase, and glutathione reductase activities and the increase in malondialdehyde content indicated that GM-induced tissue injury was mediated through oxidative reactions. In contrast, MT treatment protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by the GM treatment. Histopathological studies confirmed the renoprotective effect of MT. These results indicate that MT prevents nephrotoxicity induced by GM in rats, presumably because it is a potent antioxidant, restores antioxidant enzyme activity, and blocks NF-κB and iNOS activation in rat kidney.
Insights
Melatonin (MT) protects against gentamicin (GM)-induced kidney damage by reducing oxidative stress and apoptosis. This study shows MT
Area of Science:
- Nephrology
- Toxicology
- Biochemistry
Background:
- Gentamicin (GM) is an antibiotic known to cause nephrotoxicity.
- Oxidative stress and apoptosis play key roles in GM-induced kidney damage.
- Melatonin (MT) is a potent antioxidant with potential renoprotective properties.
Purpose of the Study:
- To investigate the protective effects of melatonin against gentamicin-induced nephrotoxicity and oxidative stress in rats.
- To explore the mechanisms by which melatonin mitigates gentamicin-induced renal damage, including its effects on apoptosis and key signaling pathways.
Main Methods:
- Four groups of rats were used: vehicle control, melatonin only, gentamicin only, and gentamicin plus melatonin.
- Nephrotoxicity was assessed by measuring serum levels of blood urea nitrogen and creatinine.
- Renal tissue apoptosis, oxidative stress markers (glutathione, malondialdehyde), and protein expression (iNOS, NF-κB, Bcl2-associated X protein, cleaved caspase-3) were analyzed.
Main Results:
- Gentamicin induced significant nephrotoxicity, characterized by elevated serum markers, increased renal tubular cell apoptosis, and upregulated pro-apoptotic proteins.
- GM treatment led to increased oxidative stress, indicated by decreased antioxidant enzyme activities and increased malondialdehyde.
- Melatonin administration significantly attenuated gentamicin-induced nephrotoxicity, reduced oxidative stress, inhibited apoptosis, and decreased the expression of iNOS and NF-κB.
Conclusions:
- Melatonin exerts significant renoprotective effects against gentamicin-induced nephrotoxicity in rats.
- Melatonin's protective mechanisms involve potent antioxidant activity, restoration of antioxidant enzyme function, and inhibition of NF-κB and iNOS activation.
- These findings highlight melatonin as a potential therapeutic agent for preventing or treating gentamicin-induced kidney injury.
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